期刊
NATURE IMMUNOLOGY
卷 7, 期 7, 页码 763-772出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1351
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- NCI NIH HHS [CA38355] Funding Source: Medline
- NIAID NIH HHS [AI46710, AI21487] Funding Source: Medline
- NIA NIH HHS [AG01743] Funding Source: Medline
T cell activation involves the orchestration of several signaling pathways, including that of the 'classical' transcription factor NF-kappa B components NF-kappa B1-RelA. The function of the 'nonclassical' NF-kappa B2-RelB pathway is less clear, although T cells lacking components of this pathway have activation defects. Here we show that mice deficient in NF-kappa B-inducing kinase have a complex phenotype consisting of immunosuppression mediated by CD25-Foxp3-memory CD4(+) cells and, in the absence of those cells, hyper-responsive naive CD4(+) T cells, which caused autoimmune lesions after adoptive transfer into hosts deficient in recombination-activating genes. Biochemical studies indicated involvement of a cell-intrinsic mechanism in which NF-kappa B2 (p100) limits nuclear translocation of NF-kappa B1-RelA and thereby functions as a regulatory 'brake' for the activation of naive T cells.
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